The hypersensitive response (HR), a form of programmed cell death (PCD), is a tightly regulated innate immune response in plants that is hypothesized to restrict pathogen growth and disease development. Although considerable efforts have been made to understand HR PCD, it remains unknown whether the retrograde pathway from the Golgi to the endoplasmic reticulum (ER) is involved. Here we provide direct genetic evidence that two Nicotiana benthamiana homologs, ERD2a and ERD2b, function as ER luminal protein receptors and participate in HR PCD. Virus-induced gene silencing (VIGS) of ERD2a and/or ERD2b caused escape of ER-resident proteins from the ER, and resulted in plants that were more sensitive to ER stress. Silencing of ERD2b delayed HR PCD induced by the non-host pathogens Xanthomonas oryzae pv. oryzae and Pseudomonas syringae pv. tomato DC3000. However, both silencing of ERD2a and co-silencing of ERD2a andERD2b exacerbated HR PCD. Individual and combined suppression of ERD2a and ERD2b exaggerated R gene-mediated cell death. Nevertheless, silencing ofERD2a and/or ERD2b had no detectable effects on bacterial growth. Furthermore, VIGS of several putative ligands of ERD2a/2b, including the ER quality control (ERQC) component genes BiP, CRT3 and UGGT, had different effects on HR PCD induced by different pathogens. This indicates that immunity-related cell death pathways are separate with respect to the genetic requirements for these ERQC components. These results suggest that ERD2a and ERD2b function as ER luminal protein receptors to ensure ERQC and alleviate ER stress, thus affecting HR PCD during the plant innate immune response.

The fungus Piriformospora indica colonizes the roots of different plants. This can be orchids, tobacco, barley or even moss. It penetrates into the roots, but does not damage the plants. On the contrary, it can even promote the growth of its plant partners. Such and other interactions between the fungus and its partners are already known to the scientific community.

Research groups from Cologne and Würzburg are now reporting a new facet of the fungus-plant relationship in Nature Communications: The researchers identified a protein with which the fungus suppresses the immune defence of the populated plants. So it makes sure that it is not attacked like disease-inducing fungi and the relationship can succeed in the long run.

The protein "Fungal Glucan Binding 1" (FGB1) prevents the plant from producing an "oxidative burst". This usually generates aggressive oxygen radicals, which destroy potential pathogens and activate the immune system of the plant.

Protein makes the plant blind to fungus structures How does the protein lame the immune response of the plant? "It binds with highly affinity and very specifically to sugar molecules that sit in the cell wall of the fungi and which are normally recognized as 'foreign' by the plant," explains Professor of Molecular Biology Alga Zuccaro from the University of Cologne. FGB1 acts like a camouflage coat and conceals the foreign sugar molecules from the immune system.

Background Among the environmental limitations that affect plant growth, viruses cause major crop losses worldwide and represent serious threats to food security. Significant advances in the field of plant–virus interactions have led to an expansion of potential strategies for genetically engineered resistance in crops during recent years. Nevertheless, the evolution of viral virulence represents a constant challenge in agriculture that has led to a continuing interest in the molecular mechanisms of plant–virus interactions that affect disease or resistance.

Scope and Conclusion This review summarizes the molecular mechanisms of the antiviral immune system in plants and the latest breakthroughs reported in plant defence against viruses. Particular attention is given to the immune receptors and transduction pathways in antiviral innate immunity. Plants counteract viral infection with a sophisticated innate immune system that resembles the non-viral pathogenic system, which is broadly divided into pathogen-associated molecular pattern (PAMP)-triggered immunity and effector-triggered immunity. An additional recently uncovered virus-specific defence mechanism relies on host translation suppression mediated by a transmembrane immune receptor. In all cases, the recognition of the virus by the plant during infection is central for the activation of these innate defences, and, conversely, the detection of host plants enables the virus to activate virulence strategies. Plants also circumvent viral infection through RNA interference mechanisms by utilizing small RNAs, which are often suppressed by co-evolving virus suppressors. Additionally, plants defend themselves against viruses through hormone-mediated defences and activation of the ubiquitin–26S proteasome system (UPS), which alternatively impairs and facilitates viral infection. Therefore, plant defence and virulence strategies co-evolve and co-exist; hence, disease development is largely dependent on the extent and rate at which these opposing signals emerge in host and non-host interactions. A deeper understanding of plant antiviral immunity may facilitate innovative biotechnological, genetic and breeding approaches for crop protection and improvement.

Positive-strand RNA viruses build extensive membranous replication compartments to support replication and protect the virus from antiviral responses by the host. These viruses require host factors and various lipids to form viral replication complexes (VRCs). The VRCs built by Tomato bushy stunt virus (TBSV) are enriched with phosphatidylethanolamine (PE) through a previously unknown pathway. To unravel the mechanism of PE enrichment within the TBSV replication compartment, in this paper, the authors demonstrate that TBSV co-opts the guanosine triphosphate (GTP)-bound active form of the endosomal Rab5 small GTPase via direct interaction with the viral replication protein. Deletion of Rab5 orthologs in a yeast model host or expression of dominant negative mutants of plant Rab5 greatly decreases TBSV replication and prevents the redistribution of PE to the sites of viral replication. We also show that enrichment of PE in the viral replication compartment is assisted by actin filaments. Interestingly, the closely related Carnation Italian ringspot virus, which replicates on the boundary membrane of mitochondria, uses a similar strategy to the peroxisomal TBSV to hijack the Rab5-positive endosomes into the viral replication compartments. Altogether, usurping the GTP-Rab5–positive endosomes allows TBSV to build a PE-enriched viral replication compartment, which is needed to support peak-level replication. Thus, the Rab family of small GTPases includes critical host factors assisting VRC assembly and genesis of the viral replication compartment.

Protein poly(ADP-ribosyl)ation (PARylation) primarily catalyzed by poly(ADP-ribose) polymerases (PARPs) plays a crucial role in controlling various cellular responses. However, PARylation targets and their functions remain largely elusive. Here, we deployed an Arabidopsis protein microarray coupled with in vitro PARylation assays to globally identify PARylation targets in plants. Consistent with the essential role of PARylation in plant immunity, the forkhead-associated (FHA) domain protein DAWDLE (DDL), one of PARP2 targets, positively regulates plant defense to both adapted and non-adapted pathogens. Arabidopsis PARP2 interacts with and PARylates DDL, which was enhanced upon treatment of bacterial flagellin. Mass spectrometry and mutagenesis analysis identified multiple PARylation sites of DDL by PARP2. Genetic complementation assays indicate that DDL PARylation is required for its function in plant immunity. In contrast, DDL PARylation appears to be dispensable for its previously reported function in plant development partially mediated by the regulation of microRNA biogenesis. Our study uncovers many previously unknown PARylation targets and points to the distinct functions of DDL in plant immunity and development mediated by protein PARylation and small RNA biogenesis, respectively.

Necrotrophic pathogens live and feed on dying tissue, but their interactions with plants are not well understood compared to biotrophic pathogens. The wheat Snn1 gene confers susceptibility to strains of the necrotrophic pathogen Parastagonospora nodorum that produce the SnTox1 protein. We report the positional cloning of Snn1 , a member of the wall-associated kinase class of receptors, which are known to drive pathways for biotrophic pathogen resistance. Recognition of SnTox1 by Snn1 activates programmed cell death, which allows this necrotroph to gain nutrients and sporulate. These results demonstrate that necrotrophic pathogens such as P. nodorum hijack host molecular pathways that are typically involved in resistance to biotrophic pathogens, revealing the complex nature of susceptibility and resistance in necrotrophic and biotrophic pathogen interactions with plants.

β-glucans are well-known modulators of the immune system in mammals but little is known about β-glucan triggered immunity in planta. Here we show by isothermal titration calorimetry, circular dichroism spectroscopy and nuclear magnetic resonance spectroscopy that the FGB1 gene from the root endophyte Piriformospora indica encodes for a secreted fungal-specific β-glucan-binding lectin with dual function. This lectin has the potential to both alter fungal cell wall composition and properties, and to efficiently suppress β-glucan-triggered immunity in different plant hosts, such as Arabidopsis, barley and Nicotiana benthamiana. Our results hint at the existence of fungal effectors that deregulate innate sensing of β-glucan in plants.

Positive-strand RNA viruses build extensive membranous replication compartments to support replication and protect the virus from antiviral responses by the host. These viruses require host factors and various lipids to form viral replication complexes (VRCs). The VRCs built by Tomato bushy stunt virus (TBSV) are enriched with phosphatidylethanolamine (PE) through a previously unknown pathway. To unravel the mechanism of PE enrichment within the TBSV replication compartment, in this paper, the authors demonstrate that TBSV co-opts the guanosine triphosphate (GTP)-bound active form of the endosomal Rab5 small GTPase via direct interaction with the viral replication protein. Deletion of Rab5 orthologs in a yeast model host or expression of dominant negative mutants of plant Rab5 greatly decreases TBSV replication and prevents the redistribution of PE to the sites of viral replication. We also show that enrichment of PE in the viral replication compartment is assisted by actin filaments. Interestingly, the closely related Carnation Italian ringspot virus, which replicates on the boundary membrane of mitochondria, uses a similar strategy to the peroxisomal TBSV to hijack the Rab5-positive endosomes into the viral replication compartments. Altogether, usurping the GTP-Rab5–positive endosomes allows TBSV to build a PE-enriched viral replication compartment, which is needed to support peak-level replication. Thus, the Rab family of small GTPases includes critical host factors assisting VRC assembly and genesis of the viral replication compartment.

Ask a developmental biologist to name the most valuable animal models for their field and they will probably put the African clawed frog, Xenopus laevis, at or near the top of their list. Ask any geneticist the same question and this species is unlikely to even make the top ten. One reason for this disparity is that X. laevis has undergone a whole-genome duplication, which makes genome assembly — an essential tool of modern genetics — extremely difficult. But on page 336, Session et al.1 report the successful sequencing of the X. laevis genome. The authors took advantage of ever-improving technologies and the hard work of a large, international consortium to complete this challenging project.

During the genome-assembly process for a diploid organism (one, like humans, that has two sets of chromosomes), a single reference chromosome sequence is generated to correspond to each chromosome pair. X. laevis, by contrast, is tetraploid — it has four sets of chromosomes, and so a reference sequence will contain two copies of most genes, instead of one. This leads to problems when using the typical shotgun approach to genome assembly, in which hundreds of millions of random short sequence reads are taken and assembled by computer into logical, continuous sequences. With a duplicated genome, it can be difficult to tell which of the two gene copies a short sequence comes from. If the sequences of the copies are too similar, the computer's assembly algorithms 'collapse' the duplicated sequence into a single copy, confounding attempts to make correct, end-to-end assemblies across all chromosomes.

Two laborious approaches that enable distinctions between duplicated chromosomes made Session and colleagues' effort successful. In the first, the authors isolated DNA from a frog and inserted long stretches into DNA constructs called bacterial artificial chromosomes (BACs). They then systematically identified 798 BACs that contained large fragments (100 kilobases or more) of DNA encoding one copy of a duplicated gene, and that could be paired with another BAC containing the other copy.

Stilbenes are central phytoalexins in Vitis, and induction of the key enzyme stilbene synthase (STS) is pivotal for disease resistance. Here, we address the potential for breeding resistance using an STS allele isolated from Chinese wild grapevine Vitis pseudoreticulata (VpSTS) by comparison with its homologue from Vitis vinifera cv. ‘Carigane’ (VvSTS). Although the coding regions of both alleles are very similar (>99% identity on the amino acid level), the promoter regions are significantly different. By expression in Arabidopsis as a heterologous system, we show that the allele from the wild Chinese grapevine can confer accumulation of stilbenes and resistance against the powdery mildew Golovinomyces cichoracearum, whereas the allele from the vinifera cultivar cannot. To dissect the upstream signalling driving the activation of this promoter, we used a dual-luciferase reporter system in a grapevine cell culture. We show elevated responsiveness of the promoter from the wild grape to salicylic acid (SA) and to the pathogen-associated molecular pattern (PAMP) flg22, equal induction of both alleles by jasmonic acid (JA), and a lack of response to the cell death-inducing elicitor Harpin. This elevated SA response of the VpSTS promoter depends on calcium influx, oxidative burst by RboH, mitogen-activated protein kinase (MAPK) signalling, and JA synthesis. We integrate the data in the context of a model where the resistance of V. pseudoreticulata is linked to a more efficient recruitment of SA signalling for phytoalexin synthesis.

Roots are increasingly recognized as key regulators of aboveground interactions between plants and other organisms. In this issue of Journal of Experimental Botany, Agut et al. (pages 5711–5723) enrich our understanding of the underground signalling mechanisms in the shoot–root–shoot (SRS) loop that regulates canopy-wide defence responses after a leaf is attacked.

The plant hormone auxin is perceived by the nuclear F-box protein TIR1 receptor family and regulates gene expression through degradation of Aux/IAA transcriptional repressors. Several studies have revealed the importance of the proteasome in auxin signalling, but details on how the proteolytic machinery is regulated and how this relates to degradation of Aux/IAA proteins remains unclear. Here we show that an Arabidopsis homologue of the proteasome inhibitor PI31, which we name PROTEASOME REGULATOR1 (PTRE1), is a positive regulator of the 26S proteasome. Loss-of-function ptre1 mutants are insensitive to auxin-mediated suppression of proteasome activity, show diminished auxin-induced degradation of Aux/IAA proteins and display auxin-related phenotypes. We found that auxin alters the subcellular localization of PTRE1, suggesting this may be part of the mechanism by which it reduces proteasome activity. Based on these results, we propose that auxin regulates proteasome activity via PTRE1 to fine-tune the homoeostasis of Aux/IAA repressor proteins thus modifying auxin activity.

Recent years have seen extensive research in the molecular underpinnings of symbiotic plant-fungal interactions. Molecular Mycorrhizal Symbiosis is a timely collection of work that will bridge the gap between molecular biology, fungal genomics, and ecology. A more profound understanding of mycorrhizal symbiosis will have broad-ranging impacts on the fields of plant biology, mycology, crop science, and ecology.

Molecular Mycorrhizal Symbiosis will open with introductory chapters on the biology, structure and phylogeny of the major types of mycorrhizal symbioses. Chapters then review different molecular mechanisms driving the development and functioning of mycorrhizal systems and molecular analysis of mycorrhizal populations and communities. The book closes with chapters that provide an overall synthesis of field and provide perspectives for future research.

Authoritative and timely, Molecular Mycorrhizal Symbiosis, will be an essential reference from those working in plant and fungal biology.

In an approaching scenario of soil nutrient depletion, root association with soil microorganisms can be key for plant health and sustainability [ 1–3 ]. Symbiotic arbuscular mycorrhizal (AM) fungi are major players in helping plants growing under nutrient starvation conditions. They provide plants with minerals like phosphate and, furthermore, act as modulators of plant growth altering the root developmental program [ 4, 5 ]. However, the precise mechanisms involved in this latter process are not well understood. Here, we show that AM fungi are able to modulate root cortex development in Medicago truncatula by activating a novel GRAS-domain transcription factor, MIG1, that determines the size of cortical root cells. MIG1 expression peaks in arbuscule-containing cells, suggesting a role in cell remodeling during fungal accommodation. Roots ectopically expressing MIG1 become thicker due to an increase in the number and width of cortical cells. This phenotype is fully counteracted by gibberellin (GA) and phenocopied with a GA biosynthesis inhibitor or by expression of a dominant DELLA (Δ18DELLA1) protein. MIG1 downregulation leads to malformed arbuscules, a phenotype rescued by Δ18DELLA1, suggesting that MIG1 intersects with the GA signaling to control cell morphogenesis through DELLA1. DELLA1 was shown to be a central node controlling arbuscule branching [ 6–8 ]. Now we provide evidence that, together with MIG1, DELLA1 is responsible for radial cortical cell expansion during arbuscule development. Our data point toward DELLA proteins being not only longitudinal root growth repressors [ 9 ] but also positive regulators of cortical radial cell expansion, extending the knowledge of how DELLAs control root growth.

Arbuscular mycorrhizal (AM) fungi associate with the vast majority of land plants, providing mutual nutritional benefits and protecting hosts against biotic and abiotic stresses. Significant progress was made recently in our understanding of the genomic organization, the obligate requirements, and the sexual nature of these fungi through the release and subsequent mining of genome sequences. Genomic and genetic approaches also improved our understanding of the signal repertoire used by AM fungi and their plant hosts to recognize each other for the initiation and maintenance of this association. Evolutionary and bioinformatic analyses of host and nonhost plant genomes represent novel ways with which to decipher host mechanisms controlling these associations and shed light on the stepwise acquisition of this genetic toolkit during plant evolution. Mining fungal and plant genomes along with evolutionary and genetic approaches will improve understanding of these symbiotic associations and, in the long term, their usefulness in agricultural settings.

Bikram Gill and colleagues report map-based cloning of Fhb1, which confers resistance to Fusarium head blight in wheat. They show that the PFT gene at Fhb1 confers resistance and encodes a chimeric lectin with agglutinin domains and a pore-forming toxin domain, identifying a new type of durable plant-resistance gene.

In an approaching scenario of soil nutrient depletion, root association with soil microorganisms can be key for plant health and sustainability [ 1–3 ]. Symbiotic arbuscular mycorrhizal (AM) fungi are major players in helping plants growing under nutrient starvation conditions. They provide plants with minerals like phosphate and, furthermore, act as modulators of plant growth altering the root developmental program [ 4, 5 ]. However, the precise mechanisms involved in this latter process are not well understood. Here, we show that AM fungi are able to modulate root cortex development in Medicago truncatula by activating a novel GRAS-domain transcription factor, MIG1, that determines the size of cortical root cells. MIG1 expression peaks in arbuscule-containing cells, suggesting a role in cell remodeling during fungal accommodation. Roots ectopically expressing MIG1 become thicker due to an increase in the number and width of cortical cells. This phenotype is fully counteracted by gibberellin (GA) and phenocopied with a GA biosynthesis inhibitor or by expression of a dominant DELLA (Δ18DELLA1) protein. MIG1 downregulation leads to malformed arbuscules, a phenotype rescued by Δ18DELLA1, suggesting that MIG1 intersects with the GA signaling to control cell morphogenesis through DELLA1. DELLA1 was shown to be a central node controlling arbuscule branching [ 6–8 ]. Now we provide evidence that, together with MIG1, DELLA1 is responsible for radial cortical cell expansion during arbuscule development. Our data point toward DELLA proteins being not only longitudinal root growth repressors [ 9 ] but also positive regulators of cortical radial cell expansion, extending the knowledge of how DELLAs control root growth.

To explore the origins and consequences of tetraploidy in the African clawed frog, we sequenced the Xenopus laevis genome and compared it to the related diploid X. tropicalis genome. We characterize the allotetraploid origin of X. laevis by partitioning its genome into two homoeologous subgenomes, marked by distinct families of ‘fossil’ transposable elements. On the basis of the activity of these elements and the age of hundreds of unitary pseudogenes, we estimate that the two diploid progenitor species diverged around 34 million years ago (Ma) and combined to form an allotetraploid around 17–18 Ma. More than 56% of all genes were retained in two homoeologous copies. Protein function, gene expression, and the amount of conserved flanking sequence all correlate with retention rates. The subgenomes have evolved asymmetrically, with one chromosome set more often preserving the ancestral state and the other experiencing more gene loss, deletion, rearrangement, and reduced gene expression.

Pathogenesis-related proteins played a pioneering role fifty years ago in the discovery of plant innate immunity as a set of proteins that accumulated upon pathogen challenge. The most abundant of these proteins, PATHOGENESIS-RELATED 1 (PR-1) encodes a small antimicrobial protein that has become, as a marker of plant immune signaling, one of the most referred to plant proteins. However, the biochemical activity and mode of action of PR-1 proteins has remained elusive. Here, we provide genetic and biochemical evidence for the capacity of PR-1 proteins to bind sterols and demonstrate that the inhibitory effect on pathogen growth is caused by sterol sequestration from pathogens. In support of our findings, sterol-auxotroph pathogens such as the oomycete Phytophthora are particularly sensitive to PR-1 whereas sterol-prototroph fungal pathogens become highly sensitive only when sterol-biosynthesis is compromised. Our results are in line with previous findings showing that plants with enhanced PR-1 expression are particularly well protected against oomycete pathogens.

It is an apparent conundrum how plants evolved effector-triggered immunity (ETI), involving programmed cell death (PCD), as a major defence mechanism against biotrophic pathogens, because ETI-associated PCD could leave them vulnerable to necrotrophic pathogens that thrive on dead host cells. Interestingly, during ETI, the normally antagonistic defence hormones, salicylic acid (SA) and jasmonic acid (JA) associated with defence against biotrophs and necrotrophs respectively, both accumulate to high levels. In this study, we made the surprising finding that JA is a positive regulator of RPS2-mediated ETI. Early induction of JA-responsive genes and de novo JA synthesis following SA accumulation is activated through the SA receptors NPR3 and NPR4, instead of the JA receptor COI1. We provide evidence that NPR3 and NPR4 may mediate this effect by promoting degradation of the JA transcriptional repressor JAZs. This unique interplay between SA and JA offers a possible explanation of how plants can mount defence against a biotrophic pathogen without becoming vulnerable to necrotrophic pathogens.

Mycorrhizal symbioses are one of the most ubiquitous inter-organism relationships on the Earth, and particularly so in the terrestrial environment (Smith and Read, 2008). These relationships have major roles in the functioning of ecosystems, and are of large importance for humans via biodiversity maintenance, contribution to biogeochemical cycles, food and timber production, and other benefits (Gianinazzi et al., 2010, van der Heijden et al., 2015 and Bender et al., 2016). Thus, thorough understanding of the diversity of mycorrhizal interactions—diversity of interacting plants, fungi, and diversity of mycorrhizal types—and ultimately on mycorrhizal functioning is timely.

This Special Issue contains six papers that were presented as oral or poster presentations at the 8th International Conference on Mycorrhizas (ICOM8) in Flagstaff, Arizona, August 3-7th 2015 (Chagnon et al., 2016), including presentations at the opening symposium of the conference, “Diversity and biogeography of mycorrhizal fungi”. The papers span an array of topics on mycorrhizal diversity: mycorrhizal types from arbuscular mycorrhiza (Lekberg and Waller, 2016 and Öpik and Davison, 2016) to ectomycorrhiza (Lamit et al., 2016) and ericoid mycorrhiza (Leopold, 2016), the distribution of mycorrhizal types across the USA (Swaty et al., 2016), the diversity of mycorrhizal partners (Lekberg and Waller, 2016, Öpik and Davison, 2016 and Swaty et al., 2016), and both theoretical (Chagnon, 2016) and empirical (Lekberg and Waller, 2016) approaches to disentangling host-fungal relationships across a range of genetic scales (Lamit et al., 2016). This fine sample of research topics, results, ideas and overviews reflects the remarkable contributions of mycorrhizal researchers to a breadth of research areas: from taxonomy to genetics and physiology, spatial scales ranging from cells to ecosystems, from individuals (autecology) to geochemical cycles, and the development of methodological approaches and ecological theory (e.g., Bever et al., 2010, van der Heijden et al., 2015, Moeller and Neubert, 2016 and Peay, 2016).

Plant defense responses to pathogens involve massive transcriptional reprogramming. Recently, differential coexpression analysis has been developed to study the rewiring of gene networks through microarray data, which is becoming an important complement to traditional differential expression analysis. Using time-series microarray data of Arabidopsis thaliana infected with Pseudomonas syringae, we analyzed Arabidopsis defense responses to P. syringae through differential coexpression analysis. Overall, we found that differential coexpression was a common phenomenon of plant immunity. Genes that were frequently involved in differential coexpression tend to be related to plant immune responses. Importantly, many of those genes have similar average expression levels between normal plant growth and pathogen infection but have different coexpression partners. By integrating the Arabidopsis regulatory network into our analysis, we identified several transcription factors that may be regulators of differential coexpression during plant immune responses. We also observed extensive differential coexpression between genes within the same metabolic pathways. Several metabolic pathways, such as photosynthesis light reactions, exhibited significant changes in expression correlation between normal growth and pathogen infection. Taken together, differential coexpression analysis provides a new strategy for analyzing transcriptional data related to plant defense responses and new insights into the understanding of plant-pathogen interactions.

Asian soybean rust (ASR), caused by the fungus Phakopsora pachyrhizi, is one of the most economically important crop diseases, but is only treatable with fungicides, which are becoming less effective owing to the emergence of fungicide resistance. There are no commercial soybean cultivars with durable resistance to P. pachyrhizi, and although soybean resistance loci have been mapped, no resistance genes have been cloned. We report the cloning of a P. pachyrhizi resistance gene CcRpp1 (Cajanus cajan Resistance against Phakopsora pachyrhizi 1) from pigeonpea (Cajanus cajan) and show that CcRpp1 confers full resistance to P. pachyrhizi in soybean. Our findings show that legume species related to soybean such as pigeonpea, cowpea, common bean and others could provide a valuable and diverse pool of resistance traits for crop improvement.

Asian soybean rust (ASR), caused by the fungus Phakopsora pachyrhizi, is one of the most economically important crop diseases, but is only treatable with fungicides, which are becoming less effective owing to the emergence of fungicide resistance. There are no commercial soybean cultivars with durable resistance to P. pachyrhizi, and although soybean resistance loci have been mapped, no resistance genes have been cloned. We report the cloning of a P. pachyrhizi resistance gene CcRpp1 (Cajanus cajan Resistance against Phakopsora pachyrhizi 1) from pigeonpea (Cajanus cajan) and show that CcRpp1 confers full resistance to P. pachyrhizi in soybean. Our findings show that legume species related to soybean such as pigeonpea, cowpea, common bean and others could provide a valuable and diverse pool of resistance traits for crop improvement.

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